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Bone and joint tuberculosis

author: Jason Stout, MD

section editor: John Bernardo, MD
deputy editor: Elinor L Baron, MD, DTMH

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jul 2023.

This topic last updated: Jun 27, 2022.

INTRODUCTION

Skeletal tuberculosis (TB) refers to TB involvement of the bones and/or joints. It is an ancient disease;
features of spinal TB have been identified in Egyptian mummies dating back 9000 years [1,2], and analysis
of 483 pre-Columbian skeletons in Chile showed lesions consistent with bony TB in 2 percent of cases [3].
Subsequently, molecular studies have established the presence of Mycobacterium tuberculosis complex
deoxyribonucleic acid (DNA) in ancient bony specimens [2,4].

Clinical issues related to skeletal TB will be reviewed here. Other aspects of TB are discussed separately.
(See related topics.)

EPIDEMIOLOGY

Worldwide, skeletal TB accounts for 10 to 35 percent of cases of extrapulmonary TB (9.6 percent of United
States extrapulmonary cases [n=185] and 2.0 percent of all United States TB cases reported in 2017) [5-10].
Reported rates of extrapulmonary TB are higher among immigrants from highly endemic areas to
developed countries; this may be due in part to immigration screening procedures for pulmonary TB [11].
One retrospective review of skeletal TB between 1980 and 1994 in France noted 103 cases of spinal TB; 68
percent of patients were foreign born, the majority from Africa [12]. The proportion of skeletal TB among
individuals with human immunodeficiency virus (HIV) infection is comparable with the proportion of
skeletal TB among individuals without HIV infection [13,14].

The most common form of skeletal TB is Pott disease, a disease of the spine; this entity comprises
approximately half of musculoskeletal TB cases. The next most common form of musculoskeletal TB is
tuberculous arthritis, followed by extraspinal tuberculous osteomyelitis [15].

PATHOGENESIS

During primary M. tuberculosis infection, bacillemia may lead to seeding of organisms in bone and/or
synovial tissue. In most cases, small foci of infection are confined by local adaptive immune processes, and
infection is subclinical. Following primary infection, reactivating foci are usually contained by the cellular
immune response. CD4 and CD8 lymphocytes play important roles, as does interferon-gamma [16]. The
likelihood of reactivation of infection with progression to clinically apparent disease increases when local
immune defenses fail, as in the setting of malnutrition, advancing age, HIV infection, or advanced kidney
disease [17].

Active TB disease can develop immediately or after decades of latent infection. In highly endemic regions,
musculoskeletal TB usually manifests clinically in the year following primary lung infection and therefore
occurs more frequently in relatively young patients [18]. Outside highly endemic areas, musculoskeletal TB
is more commonly associated with late reactivation of infection and occurs mainly in adults.

Two types of bone and joint involvement associated with TB infection have been described: the caseous
exudative type and the granular type [19]. The caseous exudative type is characterized by bone
destruction, local swelling, abscess formation, sinus formation, and constitutional symptoms; it occurs
most often in children. The granular type is more insidious and less destructive than the caseous exudative
type, and abscess formation is less common; it occurs most often in adults. However, host-parasite
interactions in TB are dynamic, often with mixed patterns and transitions along a continuum [20].

Rarely, bones and joints are involved in contiguous spread of TB from another site. Contiguous spread
from an apical pulmonary focus of active TB, for example, can lead to atlantoaxial TB, involving the joint
between the first and second cervical vertebrae [21].

CLINICAL MANIFESTATIONS

Forms of skeletal TB include spondylitis (Pott disease), arthritis, and osteomyelitis. From published series
of spinal TB, there is wide variation in reported rates of active concomitant pulmonary TB at the time of
diagnosis of the spinal TB [12,22,23]. The largest report series including nearly 700 cases had the lowest
reported rate (2.7 percent) [23]. The proportion is likely to be similarly variable for other TB bone and joint
infections, but series are too small to provide reliable data. Virtually any bone can be infected with M.
tuberculosis. The diagnosis may be delayed when unusual bones such as the hyoid or digits are infected or
when multifocal bony involvement is present.

Spondylitis (Pott disease) — Tuberculous spondylitis (Pott disease) most commonly affects the lower
thoracic and upper lumbar region; involvement of cervical and upper thoracic region is less common
[24,25]. Progression of infection generally begins with inflammation of the anterior aspect of intervertebral
joints; typically, it spreads behind the anterior ligament to involve the adjacent vertebral body. Once two
adjacent vertebrae are involved, infection enters the adjoining intervertebral disc space. This tends to
occur later in Pott disease than in bacterial vertebral osteomyelitis and may have the radiographic
appearance of relative disc sparing. Eventually, the avascular disc tissue dies; there is vertebral narrowing
and subsequent vertebral collapse. Gibbus deformity, a form of structural kyphosis, distorts spinal canal
anatomy ( image 1). The spinal cord is then at risk of compression resulting in paraplegia, especially with
involvement of the mid-thoracic region where the spinal canal is relatively "tight" around the cord [26].
Occasionally, late-onset paraplegia occurs due to osteophytes and other chronic degenerative changes at
a site of prior infection. Formation of a "cold abscess" (soft tissue mass) at the site is common.
Noncontiguous spinal disease (eg, disease at more than one level) is uncommon, although in one South
African series it was described in 16 of 98 cases [27].

The most common symptom is local pain, which increases in severity over weeks to months, sometimes in
association with muscle spasm and rigidity. The muscle spasm can extend beyond the diseased area. In
some cases, a characteristic erect posture and "alderman's" gait may be observed in which the patient
walks with short, deliberate steps to avoid jarring of the spine [28]. Constitutional symptoms such as fever
and weight loss are present in less than 40 percent of cases [13,22,29-31].

The diagnosis of Pott disease is frequently delayed as a result of its subacute course, especially in regions
where the incidence of TB is relatively low [13,22]. In endemic areas, the clinical presentation also tends to
be relatively late due to limited access to medical care; in these settings, patients have symptoms and
signs of cord compression at the time of diagnosis in 40 to 70 percent of cases [22,32]. Thus, late diagnosis
is a major factor in determining the outcome of the disease [33].

Arthritis

Infectious — Tuberculous arthritis can occur in virtually any joint, but it tends to occur in the hip or the
knee; usually, it is monoarticular. However, multifocal lesions are reported in 10 to 15 percent of cases in
resource-limited countries [34]. Hip involvement is the most common presentation, the most difficult to
diagnose, and the most debilitating [6]. Clinical manifestations include swelling, pain, and/or loss of joint
function that progresses over weeks to months. The joint is generally "cold" (eg, erythema, warmth, and
other signs of acute infection are usually absent). Constitutional symptoms, fever, and weight loss occur in
only about 30 percent of cases [29].

Patients who present late in the course of disease often have evidence of joint destruction including local
deformity and restricted range of motion. Some patients with advanced disease have draining sinuses.
Granulomatous changes typically accompany synovial proliferation in tuberculous arthritis, with joint
effusion and erosion of cartilage. The consequences are slowly progressive destruction, disorganization of
joint architecture, and potential deformity.

Some data suggest that total hip replacement in the setting of active TB is acceptable if undertaken in
association with appropriate debridement and antituberculous therapy [35].

Inflammatory (Poncet disease) — Poncet disease is an acute symmetric polyarthritis involving large and
small joints associated with active extrapulmonary, pulmonary, or miliary TB. In general, there is
inflammation of the involved joints but no objective evidence of active TB [36-39]. Poncet disease is
relatively rare, and the pathogenesis is unclear; it is probably immune mediated [38]. HIV coinfection is
also a risk factor [40,41]. The arthritis generally resolves within a few weeks of initiation of anti-TB therapy,
with no residual joint destruction [37,42].

Prosthetic joint infection — Rarely, M. tuberculosis can cause infection at the site of a prosthetic joint
[43]. Diagnosis has been described at the time of initial arthroplasty as well as subsequent to hardware
placement [44].

For cases in which TB is identified at the time of initial arthroplasty, the diagnosis is typically a surprise to
the surgeon who sends abnormal-appearing bone for histopathologic examination or culture at the time
of joint replacement. These patients generally have a favorable outcome after standard antituberculous
chemotherapy, even if the joint prosthesis is not removed [44].

For cases in which infection is identified following hardware placement, a dormant nidus of infection
reactivates, and patients subsequently present with clinical findings of an infected prosthesis. These
patients often have painful, malfunctioning prostheses, and hardware removal is required for cure. Some
patients with late-onset tuberculous prosthetic joint infections have coexisting bacterial infection that may
mask or obscure the underlying coinfection with M. tuberculosis.

Osteomyelitis — In addition to tuberculous vertebral osteomyelitis (Pott disease), tuberculous

osteomyelitis can occur in virtually any bone, including the ribs, skull, tubular bones of the hands and feet
(dactylitis), wrist, phalanx, pelvis, and long bones. The onset is often insidious but, in rare cases, the onset
may be acute or subacute [45]. Typically, osteomyelitis occurs at a single site. However, rarely bony
involvement can be multifocal. The location and presentation can be variable as illustrated by the following
case reports:

● Sternal osteomyelitis due to M. tuberculosis may follow coronary artery bypass surgery [46] as a
presentation of underlying mediastinal TB [47] or as primary sternal osteomyelitis [48].
● Bony TB of the rib may present as a breast mass or chest wall mass [49,50].
● TB of the small bones of the hand can occur spontaneously in patients with no clinical signs of
pulmonary TB [51].
● Tuberculous mastoiditis can extend into the skull and produce facial nerve palsy [52].
● Lytic bony tubercular lesions in areas as unusual as the symphysis pubis, sacroiliac joint, and elbow
can be misdiagnosed as metastatic malignancy [53].

In some cases, bony infection may spread to contiguous soft tissues or even adjacent joints. Rarely,
involvement of multiple bones may be associated with erroneous diagnosis of metastatic malignancy [54-
56].

An antecedent history of trauma may lead to diagnostic confusion; TB can develop in a bone or joint
injured by previous trauma or surgery. Tuberculous osteomyelitis frequently presents as a "cold abscess"
with swelling, modest erythema or pain, and little or no local warmth [15]. Spontaneous drainage may
occur.

Other clinical manifestations — Musculoskeletal TB can occur as an abscess in the epidural space

(creating pressure on the spinal cord), as an extraspinal soft tissue mass (eroding ribs and adjacent
structures), or as a psoas abscess (which can track down to the groin). (See "Psoas abscess".)

Radiography — Radiographic imaging can be useful to identify and establish the anatomy of

musculoskeletal TB, although there are no pathognomonic radiographic findings [57].

In the setting of tuberculous spondylitis (Pott disease), radiographic abnormalities are usually first
observed in the anterior aspect of a vertebral body, with demineralization of the end plate and loss of
definition of the bony margin [58]. Subsequently, the opposing vertebra becomes involved and, in some
cases, a paravertebral abscess may be seen. Involvement of contiguous vertebrae is common, although it
is not uncommon to see noncontiguous spinal TB at multiple levels. As infection progresses, the disc space
becomes obliterated with anterior wedging and angulation. Reactive sclerotic changes remain localized
and the remainder of the vertebral structures is often spared ( image 2).

In some patients, spinal TB presents with osteolytic lesions in the absence of disc space involvement; these
lesions may occur at multiple sites. In one study of 103 French patients with spinal TB, no disc involvement
was observed in about half of cases; plain radiographs demonstrated osteolytic lesions and multiple
involved sites [12].

In the setting of tuberculous arthritis, local soft tissue swelling, osteopenia, and bone destruction (with
relative preservation of cartilage space) are observed. Subsequent findings include structural collapse,
sclerotic changes, and soft tissue calcification ( image 3). In some cases, Phemister triad may be
observed: juxta-articular osteopenia, peripherally located osseous erosions, and gradual narrowing of the
joint space ( image 4) [59,60].

In the setting of tuberculous osteomyelitis in children, cystic changes may be seen in the metaphyses of
long bones and in flat bones, such as the skull. In tuberculous osteomyelitis involving a hand or foot,
phalangeal bone(s) may have a ballooned appearance.

Computerized tomography, myelography, and magnetic resonance imaging (MRI) are all useful tools in the
diagnosis of musculoskeletal TB [24,61-65]. MRI is particularly valuable in demonstrating soft tissue
extension and encroachment on nearby vital structures, such as the spinal cord ( image 5 and image 6
and image 7 and image 8) [66,67].

Chest radiography is not a sensitive test for the diagnosis of skeletal TB since there is no evidence of active
chest disease in the majority of cases [5,15,22,68]. However, chest radiography should be obtained since it
may inform decisions regarding isolation, and collection of sputum specimens for mycobacterial culture
should be attempted as the organism can sometimes be isolated from sputum despite a normal chest
radiograph. The diagnosis of skeletal TB should be considered in patients with focal bony or joint
abnormalities and a chest radiograph compatible with old or active TB. (See "Diagnosis of pulmonary
tuberculosis in adults".)

DIAGNOSIS

General principles — The greatest challenge in diagnosis of skeletal TB is to consider the diagnosis,

especially since there is no evidence of active chest disease in the majority cases. In addition, delays in
diagnosis are common given the indolent nature of tuberculous bone and joint disease [69]. Clinical clues
usually come from the history, which should include questions about the country of origin and history of
prior known or possible TB infection or contact. In addition, the diagnosis of skeletal TB may be
overlooked in patients with HIV infection and relatively high CD4 counts and no other signs or symptoms
of TB.

The diagnosis of musculoskeletal TB is established by microscopy and culture of infected material. Tissue
may be obtained by needle aspiration and/or biopsy; computed tomography (CT) guidance is useful in
regions where available.

Biopsy and culture — The diagnosis of musculoskeletal TB is established by microscopy and culture of

infected material [70-72]. Drug susceptibility testing of isolates is essential. Tissue may be obtained by
needle aspiration and/or biopsy. CT guidance is useful in regions where available [73,74].

The diagnosis of tuberculous arthritis can be established by synovial biopsy. Synovial fluid may be
examined [75], but findings are usually nonspecific; the white cell count can be high or low, with
preponderance of either neutrophils or lymphocytes [76].

In the setting of one or more draining sinuses, culture of this material may be useful, although, in some
cases, cultures may demonstrate colonizing bacteria or fungi that are erroneously assumed to be the
causative pathogen.

The high cost and technical demands of rapid automated growth systems and nucleic acid detection
methods often limits their use in the poorest countries with the highest incidence of TB [77]. The Xpert
MTB/RIF assay is an automated nucleic acid amplification test that can simultaneously identify M.
tuberculosis and rifampin resistance; data on use of this assay in skeletal TB are limited and the test
platform is not approved by the Food and Drug Administration in the United States for use with specimens
other than sputum. However, the available data suggest that Xpert and the more sensitive Xpert Ultra may
be useful adjuncts to diagnosis of skeletal TB, with sensitivity of 79 and 91 percent, respectively [78]. The
Xpert MTB/RIF assay is discussed further separately. (See "Diagnosis of pulmonary tuberculosis in adults".)

Additional issues related to diagnostic microbiology are discussed further separately. (See "Diagnosis of
pulmonary tuberculosis in adults".)

Differential diagnosis — The differential diagnosis of skeletal TB includes subacute or chronic infections

due to pathogens or diseases such as Staphylococcus aureus osteomyelitis, brucellosis, melioidosis,
actinomycosis, candidiasis, and histoplasmosis, depending upon epidemiologic factors. Multifocal bone
involvement may be confused for metastatic malignancy.

The differential diagnosis of Pott disease includes degenerative disc and facet joint disease,
spondyloarthropathy, vertebral body collapse due to osteopenia (with a variety of causes such as
osteoporosis and chronic corticosteroid therapy), pyogenic spinal infection, and malignancy. Each of these
can present with similar clinical features; the main challenge for diagnosis of TB is consideration of the
diagnosis. Most of these conditions can be distinguished with imaging studies where available.

TREATMENT

General approach — Treatment of musculoskeletal TB consists of antimicrobial therapy. In some cases,

surgical intervention is also warranted.

Antimicrobial therapy — The approach to selection of antituberculous therapy for treatment of

musculoskeletal TB is generally the same as that for pulmonary TB. The drug regimen may require
modification based on concurrent medications (eg, HIV coinfection) or drug resistance. These issues are
discussed in detail separately. (See "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant
adults without HIV infection" and "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant
adults with HIV infection: Initiation of therapy" and "Treatment of drug-resistant pulmonary tuberculosis in
adults".)

The optimal duration of therapy for treatment of musculoskeletal TB is uncertain. For most patients
receiving first-line agents, six to nine months of therapy is sufficient [79]. A longer duration of therapy (9 to
12 months) is warranted for patients on regimens that do not include rifampin and/or for patients with
extensive or advanced disease, particularly if it is difficult to assess the response to therapy [79,80].

Data are limited on the optimal drug regimen and duration for treatment of musculoskeletal infections
due to drug-resistant M. tuberculosis. In one small series, 14 of 15 patients were cured with combined
medical/surgical therapy (eight patients) or medical therapy alone (seven patients). Treatment was
continued for 18 to 24 months; follow-up ranged from 5 months to 4.5 years [81].

Previously, longer therapeutic courses (12 to 18 months) have been favored for musculoskeletal TB
because of concerns about poor drug penetration into osseous and fibrous tissues. However, several
studies have shown that six- to nine-month regimens containing rifampin are at least as effective as longer
courses without rifampin [82-87]. The efficacy of shorter-course therapy is illustrated by the following:

● A large prospective cohort study in Hong Kong demonstrated that 6 months of antituberculous
therapy combined with surgery (radical resection of the lesion and insertion of autologous bone
grafts) was comparable in efficacy with 9 to 18 months of antituberculous therapy alone [82].

● In three randomized trials of short-course chemotherapy for spinal TB in Hong Kong, India, and
Korea reported after five years of follow-up, six- and nine-month regimens with isoniazid and
rifampin produced comparable results with 18 months of isoniazid with either ethambutol or para-
aminosalicylic acid [85].

● In a randomized trial of 203 Korean patients comparing four different treatment regimens [(1)
isoniazid plus rifampin for six months, (2) isoniazid plus rifampin for nine months, (3) isoniazid plus
ethambutol or para-aminosalicylic acid for nine months, or (4) isoniazid plus ethambutol or para-
aminosalicylic acid for 18 months], a favorable outcome was achieved in 77 percent of cases after
three years from the start of therapy; those who received the nine-month regimen with isoniazid plus
ethambutol or para-aminosalicylic acid required additional treatment [86].

One small retrospective study from the United Kingdom did report a high rate of relapse with a six-month
course of therapy (62 percent); no relapse was observed among patients who received nine months of
treatment [87]. In contrast, a Chinese study reported that, in selected patients and combined with
appropriate surgical intervention, ultra-short-course therapy of 4.5 months was as successful as a 9-month
course and associated with fewer side effects [88].

Surgery — Surgical intervention is warranted for patients in the following circumstances [26,50,89,90]:

● Patients with spinal disease and advanced neurological deficits

● Patients with spinal disease and worsening neurological deficits progressing while on appropriate
therapy
● Patients with spinal disease and kyphosis >40 degrees at the time of presentation
● Patients with chest wall cold abscess

Forms of surgical intervention may include decompression, use of hardware for stabilization of spine,
abscess drainage, and/or debridement of infected material [25,90]. For the most part, surgical intervention
is safe and sometimes effective in improving neurological deficits; various approaches have been
described, depending on site of infection and related abscess formation [91-93]. In some circumstances,
reconstructive surgery may be important once antimicrobial therapy has been completed [5]. Hardware is
rarely needed for stabilization of debrided bony lesions [94]. Minimally invasive surgical approaches such
as video-assisted thoracoscopic anterior surgery have been used successfully to manage patients with
neurological symptoms and/or extensive bony destruction involving the thoracic or lumbar spine [95].

The role of surgery in treatment of other presentations of musculoskeletal TB is not always clear [96]. In
one retrospective review of 70 adults with thoracic spinal TB in India, medical therapy alone was successful
in 69 of 70 patients (mean follow-up of 40 months) [89]. Criteria for exclusion included advanced
neurologic deficits, worsening neurologic deficits while on antituberculous therapy, and kyphosis greater
than 40 degrees on presentation. Abscess was observed on presentation in 44 patients (21 of which were
epidural), and 7 patients had signs of cord compression at the time of presentation. Routine surgical
intervention is not warranted [94,97].

Similar results were noted in a retrospective analysis of 52 children with TB of the knee [98]. The outcome
of medical therapy without synovectomy was excellent in children who presented with signs and
symptoms of synovitis as long as the joint space was normal.

Monitoring clinical response — The response to therapy may be monitored by clinical indicators such as
pain, constitutional symptoms, mobility, and neurologic findings. Typically, responses to therapy are
relatively slow (several months). The role of inflammatory markers in monitoring the response to TB
therapy is limited. It is not useful to perform serial radiographs since radiographic findings may appear to
progress during appropriate treatment [99].

In one study of 43 patients with Pott paraplegia, the most important prognostic factor that predicted six-
month outcome included muscle power, paraplegia score, sensory-evoked potentials, and motor-evoked
potentials [100]. Patients with mild weakness and lower paraplegia scores were more likely to recover
completely by six months than patients with more severe prognostic indicators.

For patients on antituberculous therapy for skeletal TB in the setting of antiretroviral treatment (ART) for
HIV infection, it is important to monitor for immune reconstruction inflammatory syndrome (IRIS). IRIS
typically presents with paradoxical progression of TB clinical manifestations and constitutional symptoms
in the first few weeks following initiation of ART. In the setting of skeletal TB, new clinical manifestations
may appear and/or resolved manifestations may reappear. IRIS is discussed further separately. (See
"Immune reconstitution inflammatory syndrome".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions around the
world are provided separately. (See "Society guideline links: Diagnosis and treatment of tuberculosis".)

SUMMARY AND RECOMMENDATIONS

● Skeletal tuberculosis (TB) refers to TB involvement of the bones and/or joints. Musculoskeletal TB
accounts for 10 to 35 percent of cases of extrapulmonary TB and for almost 2 percent of TB cases
overall. The proportion of skeletal TB among individuals with HIV infection is comparable with the
proportion of skeletal TB among individuals without HIV infection. (See 'Epidemiology' above.)

● Tuberculous spondylitis (Pott disease) is the most common form of skeletal TB; it usually affects the
lower thoracic and upper lumbar region. Infection begins with inflammation of the intervertebral
joints and can spread to involve the adjacent vertebral body. Once two adjacent vertebrae are
involved, infection can involve the adjoining intervertebral disc space, leading to vertebral collapse.
Subsequent kyphosis can lead to cord compression and paraplegia. (See 'Spondylitis (Pott disease)'
above.)

● The most common symptom of tuberculous spondylitis (Pott disease) is local pain, which increases in
severity over weeks to months, sometimes in association with muscle spasm and rigidity. A
characteristic erect posture and "alderman's" gait may be observed in which the patient walks with
short, deliberate steps to avoid jarring of the spine. Constitutional symptoms such as fever and
weight loss are relatively uncommon. (See 'Spondylitis (Pott disease)' above.)

● Tuberculous arthritis tends to occur in the hip or the knee and is usually monoarticular. Clinical
manifestations include swelling, pain, and/or loss of joint function that progresses over weeks to
months. The joint is generally "cold" (eg, erythema, warmth, and other signs of acute infection are
usually absent). (See 'Arthritis' above.)

● Tuberculous osteomyelitis can occur in virtually any bone, including the ribs, skull, phalanx, pelvis,
and long bones. Typically, osteomyelitis occurs at a single site. The onset is often insidious but, in rare
cases, the onset may be acute or subacute. Tuberculous osteomyelitis frequently presents as a "cold
abscess" with swelling, modest erythema or pain, and little or no local warmth. (See 'Osteomyelitis'
above.)

● The diagnosis of musculoskeletal TB is established by microscopy and culture of infected material.

Tissue may be obtained by needle aspiration and/or biopsy; guidance with computed tomography or
ultrasound to obtain tissue is useful in regions where available. Radiographic imaging can be useful
to identify and establish the anatomy of musculoskeletal TB, although there are no pathognomonic
radiographic findings. (See 'Diagnosis' above.)

● Treatment of musculoskeletal TB consists of antituberculous therapy. The approach to selection of

therapy for treatment of musculoskeletal TB is generally the same as that for pulmonary TB and is
discussed in detail separately. (See "Treatment of drug-susceptible pulmonary tuberculosis in
nonpregnant adults without HIV infection" and "Treatment of drug-susceptible pulmonary
tuberculosis in nonpregnant adults with HIV infection: Initiation of therapy" and "Treatment of drug-
resistant pulmonary tuberculosis in adults".)

● The optimal duration of therapy for treatment of musculoskeletal TB is uncertain. For patients
receiving treatment with first-line agents in the absence of extensive or advanced disease, we
suggest six months of therapy (rather than 9 or 12 months) (Grade 2B). A longer duration of therapy
(9 to 12 months) is warranted for patients on regimens that do not include rifampin and/or for
patients with extensive or advanced disease. (See 'Antimicrobial therapy' above.)

● Surgical intervention is warranted for patients with spinal disease and advanced neurological deficits
or worsening neurological deficits progressing while on appropriate therapy, as well as for patients
with spinal disease and kyphosis >40 degrees at the time of presentation. (See 'Surgery' above.)

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